Giuseppina Tesco, MD, PhD
Giuseppina Tesco, MD, PhD, Assistant Professor, Genetics and Aging Research Unit, Mass General Institute for Neurodegenerative Disease (MIND), Massachusetts General Hospital, Charlestown, Massachusetts.
Research demonstrates that head trauma increases the likelihood of developing dementia, and a story that has been in the sports pages offers anecdotal evidence: Some football players seem to be developing dementia at an unusually early age. The NFL has responded with an expanded disability package, which includes the “88 plan” — named after Baltimore Colts player John Mackey (age 66) who wore 88 on his jersey and who was diagnosed at around age 60 with fronto-temporal dementia. That’s helpful, I guess — but far better to learn how to keep this from happening in the first place.
Truth is, it’s been evident for some time that head injury as well as stroke contributes to the risk of Alzheimer’s disease (AD)… and you don’t have to be a football player or a prizefighter to sustain a head injury. The latest research from Massachusetts General Hospital adds more to our understanding of how such injuries set the stage for AD. Hopefully, this will help doctors develop therapies that can reduce the long-term risks of those who’ve had head injuries or a stroke.
The death of brain cells from both head injury and stroke boosts levels of amyloid-beta protein, which is key in facilitating the formation of senile plaque in people with Alzheimer’s disease. Both head injury and stroke set into motion a series of potentially destructive biochemical events that increase amyloid production in the brain, explains researcher Giuseppina Tesco, MD, PhD. At Massachusetts General Hospital in Charlestown, she and her colleagues set out to find why this happens. In their lab researchers have now pinpointed the process by which one protein (called GGA3) helps keep plaque-forming amyloid-beta protein in check, therefore perhaps reducing the likelihood Alzheimer’s will develop. They found that GGA3 regulates the activity of beta-secretase, one of the enzymes involved in the production of the amyloid-beta protein. Head trauma or stroke destroys GGA3. As a consequence, beta-secretase activity increases, enhancing the production of the beta-amyloid protein. This research was published in the June 7, 2007, issue of the journal Neuron.
These findings suggest that new therapies based on preserving the function of GGA3 could slow or halt those destructive biochemical events after strokes and head trauma that lead to beta-amyloid production, says Dr. Tesco. This discovery might prove especially beneficial for older people, in whom strokes and transient ischemic attacks (TIAs, or “mini-strokes”) are more common, in addition to being helpful in preventing later development of AD in people who suffered traumatic brain injury. Dr. Tesco envisions one possible future therapy will shield an already-injured brain by providing protection for the protein GGA3, thus preventing or reversing the post-traumatic processes that encourages amyloid plaque production and Alzheimer’s disease. Other possible applications are also under exploration. But, for now, this is another reason to take extra care to avoid possible head injury.